After reviewing an extensive literature, the World Health Organization and other health councils/organizations have concluded that there are no adverse health risks to adults or children associated with electromagnetic fields (EMFs) generated by cell phone use. However, there is little data concerning the long-term effects of EMFs on brain physiology and function. Epidemiologic studies have suggested that occupational (low frequency) EMF exposure may increase risk of Alzheimer's Disease (AD), while other studies have found that acute exposure to cell phone (high frequency) EMF has essentially no effect on cognitive function in normal individuals. To date, no controlled long-term studies of EMF effects on cognitive function have been done in humans, mice, or animal models for AD.
Another amyloid-related neurological disorder is traumatic brain injury (TBI). The primary/initial injury induced by TBI is largely unavoidable, but triggers secondary brain injury over the hours/days following injury that may be readily treatable. In both humans and animals, a key component to this secondary injury is rapid brain accumulation of the protein β-amyloid (Aβ) in as little as one day after injury. The two enzymes (b- and g-secretase) responsible for Aβ production from amyloid precursor protein (APP) are also increased in brain following TBI. Not surprisingly then, many TBI fatalities have brain Aβ aggregations (deposits) at autopy. This secondary production and accumulation of brain Aβ after TBI actives inflammatory pathways, induces oxidative damage/apoptosis, and causes neuronal loss. Since Aβ production and ensuing Aβ aggregation following TBI appear to be key mediators of brain tissue loss and resulting cognitive dysfunction, therapeutics aimed at post-TBI suppression of one or both of these processes could greatly limit secondary TBI injury and provide substantial functional recovery. In mice following experimental TBI, suppression of Aβ production (by reducing β- or g-secretase activity) lessens cognitive deficits, as well as reduces hippocampal neuronal loss. This work demonstrated that brain Aβ accumulation should be a primary therapeutic target against TBI. Unfortunately, these reductions in secretase activity were achieved through genetic manipulation and pharmacologic-level inhibition—neither of which is practical for human therapeutic intervention.